Abstract
Copper-catalyzed oxidation of low-density lipoproteins (LDL) (0.8 g protein/l LDL, 20 mumol/l CuSo4, 37 degrees C) resulted in the formation of thiobarbituric reactive substances that was substantially completed at 24 hrs whereas their formation from high-density lipoproteins (HDL) plateaued at only 25% of that amount after 8 hrs. The oxidized lipoproteins induced aggregation and increases in [Ca2+]i in washed platelets, but not in platelet-rich plasma, and these activating effects were not inhibited by aspirin or EGTA but were inhibited by both of the native lipoproteins. These results show that oxidized HDL, like oxidized LDL, have platelet activating ability and suggest that the native lipoproteins may play a crucial role in preventing the oxidized lipoprotein-mediated platelet activation.
MeSH terms
-
Aspirin / pharmacology
-
Calcium / blood
-
Copper / pharmacology
-
Copper Sulfate
-
Humans
-
In Vitro Techniques
-
Kinetics
-
Lipid Peroxidation
-
Lipoproteins / antagonists & inhibitors
-
Lipoproteins / drug effects
-
Lipoproteins / pharmacology*
-
Lipoproteins, HDL / pharmacology
-
Lipoproteins, LDL / pharmacology
-
Malondialdehyde / blood
-
Oxidation-Reduction
-
Platelet Activation / drug effects
-
Platelet Activation / physiology*
-
Platelet Aggregation / drug effects
-
Platelet Aggregation / physiology*
-
Platelet Aggregation Inhibitors / pharmacology*
-
Thiobarbituric Acid Reactive Substances / analysis
-
Thromboxane A2 / analogs & derivatives
-
Thromboxane A2 / pharmacology
-
Time Factors
Substances
-
Lipoproteins
-
Lipoproteins, HDL
-
Lipoproteins, LDL
-
Platelet Aggregation Inhibitors
-
Thiobarbituric Acid Reactive Substances
-
Malondialdehyde
-
Thromboxane A2
-
Copper
-
ONO 3708
-
Copper Sulfate
-
Aspirin
-
Calcium